K. Hong et al., Attenuation of conduction delay by ischemic preconditioning reduces ischemia-induced ventricular arrhythmias, ACT MED OKA, 53(5), 1999, pp. 233-238
Ischemic preconditioning has been acknowledged as a powerful method of decr
easing ischemic injury. However, the antiarrhythmic mechanism of ischemic p
reconditioning during ischemia is unclear. We studied the effects of ischem
ic preconditioning on arrhythmias and cardiac electrophysiology during isch
emia in Langendorff rat hearts (n = 44). in the non-preconditioned group (P
C(-); n = 24), the hearts underwent 5-min zero-flow global ischemia without
any prior ischemic preconditioning. In the preconditioned group (PC(+); n
= 20), the hearts were preconditioned by three cycles of 3-min zero-flow gl
obal ischemia and 5-min reperfusion before undergoing 5-min global ischemia
. Ischemic preconditioning reduced the incidence of ischemia-induced arrhyt
hmias (PC(-): 38.9 %, PC(+); 8.3 %, p < 0.05), shortened monophasic action
potential duration (MAPD, P < 0.05), attenuated conduction delay (conductio
n time; PC(-): 234.2%, PC(+): 173.4%, P < 0.05) and increased the ventricul
ar fibrillation threshold. Although the shortening of MAPD in PC(-) hearts
was not influenced by the presence or absence of arrhythmias, conduction ti
me prolongation at 3-min was more obvious in PC(-) hearts with arrhythmia t
han in PC(-) hearts without arrhythmia (PC(-) with arrhythmia: 220.2%, PC(-
) without arrhythmia: 190.7 %, P < 0.05). We concluded that ischemic precon
ditioning could protect the rat hearts from ischemia-induced arrhythmias an
d postulated that attenuation of conduction delay during ischemia might be
an important factor in the antiarrhythmic action of ischemic preconditionin
g.